Evidence map›Paper›PMID 36223751›Full record

ArticleCell reports2022

The tempo and mode of gene regulatory programs during bacterial infection.

Gal Avital, Felicia Kuperwaser, Andrew W Pountain, Keenan A Lacey, Erin E Zwack, Magdalena Podkowik, Bo Shopsin, Victor J Torres, Itai Yanai

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-weighted citation impact, top 27% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Gal AvitalInstitute for Computational Medicine, NYU Grossman School of Medicine, New York, NY, USA.
Felicia KuperwaserInstitute for Computational Medicine, NYU Grossman School of Medicine, New York, NY, USA.
Andrew W PountainInstitute for Computational Medicine, NYU Grossman School of Medicine, New York, NY, USA.
Keenan A LaceyDepartment of Microbiology, NYU Grossman School of Medicine, New York, NY, USA.
Erin E ZwackDepartment of Microbiology, NYU Grossman School of Medicine, New York, NY, USA.
Magdalena PodkowikDepartment of Medicine, Division of Infectious Diseases, NYU Grossman School of Medicine, New York, NY, USA.
Bo ShopsinDepartment of Microbiology, NYU Grossman School of Medicine, New York, NY, USA; Department of Medicine, Division of Infectious Diseases, NYU Grossman School of Medicine, New York, NY, USA.
Victor J TorresDepartment of Microbiology, NYU Grossman School of Medicine, New York, NY, USA.
Itai YanaiInstitute for Computational Medicine, NYU Grossman School of Medicine, New York, NY, USA; Department of Biochemistry and Molecular Pharmacology, NYU Grossman School of Medicine, New York, NY, USA. Electronic address: itai.yanai@nyulangone.org.
New York University · US

Funding

Training Program in Immunology and Inflammation.T32AI100853 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI Susan Ruth Schwab · 2012 to 2026
$4.5M
Spatiotemporal analysis of gene regulatory programs associated with GBS infection during pregnancyR01AI143290 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI RATNER, ADAM JONATHAN, YANAI, ITAI · 2019 to 2023
$3.8M
Mechanisms of MRSA intestinal colonizationR01AI140754 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SHOPSIN, BO · 2020 to 2024
$3.5M
Host-pathogen interactions during hospital adaptation of MRSAR01AI137336 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SHOPSIN, BO, YANAI, ITAI · 2019 to 2022
$3.3M
Alternatively activated macrophages during helminth infectionR01AI133977 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI TORRES, VICTOR J. · 2017 to 2021
$2.4M
NIAID NIH HHS R01 AI133977NIAID NIH HHS R01 AI137336NIAID NIH HHS R01 AI140754NIAID NIH HHS R01 AI143290NIAID NIH HHS T32 AI100853
6 · The paper itself

Abstract

Innate immune recognition of bacterial pathogens is a key determinant of the ensuing systemic response, and host or pathogen heterogeneity in this early interaction can impact the course of infection. To gain insight into host response heterogeneity, we investigate macrophage inflammatory dynamics using primary human macrophages infected with Group B Streptococcus. Transcriptomic analysis reveals discrete cellular states within responding macrophages, one of which consists of four sub-states, reflecting inflammatory activation. Infection with six additional bacterial species-Staphylococcus aureus, Listeria monocytogenes, Enterococcus faecalis, Yersinia pseudotuberculosis, Shigella flexneri, and Salmonella enterica-recapitulates these states, though at different frequencies. We show that modulating the duration of infection and the presence of a toxin impacts inflammatory trajectory dynamics. We provide evidence for this trajectory in infected macrophages in an in vivo model of Staphylococcus aureus infection. Our cell-state analysis defines a framework for understanding inflammatory activation dynamics in response to bacterial infection.

Indexed as

Bacterial InfectionsListeria monocytogenesGene Expression RegulationHost-Pathogen InteractionsHumansMacrophagesShigella flexneriCP: Molecular biologyhost-pathogen interactionsinfection trajectorymacrophage responsesingle-cell RNA-seq

Identifiers

PMID36223751
PMCPMC9741813
OpenAlexW4304608957

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.